26. McDowell, A., and Brown, W.: Visual acuity
performance of normal and chronic
focal-head irradiated monkeys. J. Genet.
Psy-chol., 96:139, 1960.
27. Burrow, G. N., Hamilton, H. B., and Hrubec, Z.: Study of adolescents exposed in utero
to the atomic bomb, Nagasaki, Japan. I.
General aspects: clinical and laboratory data. Yale J. Biol. Med., 36:430, 1964.
28. Storer, J. B.: Radiation resistance with age
in normal and irradiated populations of
mice. Radiation Res., 25:435, 1965.
29. Jablon, S., Ishida, M., and Yamasaki, M.:
Studies of the mortality of A-bomb
stir-vivors. 3. Description of the sample and mortality, 1950-1960. Radiation Res., 25: 25, 1965.
30. Jablon, S.: Unpublished data.
DISCUSSION
DR. YAMAZAKI: Our next speaker is Dr. \Vataru Sutow. I note that participants are
here from most of the studies that have
been done on effects on human beings or ionizing radiation. When, because of
me-teorological conditions, the bomb in the
Bikini area released fallout over the
Mar-shall Islands, the response of the people in
authority was immediate. The Navy and
Brookhaven National Laboratory group
within a matter of hours was mobilized.
They were airborne promptly and Dr.
Rob-ert Conard and his associates have followed
this group of people for 10 years. Dr. Sutow
was with this team and still is.
Dn. SuTow: Following the experimental detonation of a high-yield thermonuclear
device at Bikini in the Pacific Proving
Grounds on March 1, 1954, radioactive fall-out accidentally occurred on three inhabited
atolls of the Marshall Islands 100 to 200
miles east of Bikini. Eighteen people on
Ailingnae were exposed to 69 rads estimat-ed whole body gamma radiation. Sixty-four natives on Rongelap received an estimated
gamma dose of 175 rads, and 157
inhabi-tants of Utirik, 200 nautical miles away
from the explosion received about 14 rads.
In addition, the people of Ailingnae and
Rongelap were subjected to beta
irrradia-tion of the skin surfaces and to radiation
from internal deposition of detectable
amounts of radionuclides.’ All inhabitants
of these atolls were evacuated within 2
days. Utirik was considered habitable and
its people were returned to the atoll
im-mediately. Rongelap, however, was not
cleared for habitation until June 1957.
When the people were eventually
repatriat-ed they were accompanied by a large group
of relatives and former Rongelap residents.
These unexposed people have served as the
comparison population for the medical
studies. A brief summary of the positive
findings of the regularly conducted surveys
of these Marshall Island people over tile
past 11 years will be presented. These
corn-ments will be limited to the results of
cx-aminations of those who were under the
age of 20 years at the time of exposure and
whose exposures occurred on Ailingnae or
Rongelap.
Seven children were exposed on Ailing-nae and 31 Rongelap, a total of 38. In addi-tion, four children were exposed
in
utero at gestational ages between 40 and 180 days.Skin lesions and leukopenia occurred in
almost all these children. About 70% had
variable degrees of epilation. The
leuko-penia and thrombocytopenia showed
al-most complete recovery by 1 year after
cx-posure; but thereafter, over a period of 10
years post exposure, the average values
have remained slightly below those of the
comparison population.’
These studies also have demonstrated a
retardation of statural growth and osseous
development among boys exposed at ages 1
through 5 years, as compared to the
com-parison population. This retardation was
most marked among those who were less
than 18 months of age at exposure.3 The
physiologic mechanism for this delay in
stat-ural and skeletal development has not
been explained, although recent findings
suggest that hypothyroidism may be
impli-cated.4
In 1963, 9 years after exposure, the
264
children with thyroid nodules were found
in 1964. Thyroid nodules were palpated in
three more persons in 1965; two of them
were children. All of these subjects were
exposed to fallout; no thyroid nodules have
been found among the comparison group.
All six have had surgical treatment. No
his-tologic evidence of a malignant tumor was
noted among tile glands removed from the
five children. The tissue from the one adult showed papillary and follicular carcinoma.’
Protein bound iodine serum levels
re-mained in the normal range until 1965,
when two boys showed values in the
hypo-thyroid range. These developments indicate that the radiation dose from radioiodine in-ternally absorbed at the time of fallout may have been responsible for the growth
retar-dation and that the internal hazard from
fallout has been underestimated.”
REFERENCES
1. Some effects of ionizing radiation on human
beings, TID 5358 Washington, D.C. : U. S.
Atomic Energy Commission, July 1956.
2. Conard, Robert A., and Hicking, A.: Medical
findings in Marshallese people exposed to
fallout radiation. J.A.M.A., 192:457, 1965.
3. Sutow, W. W., Conard, R. A., and Griffith,
K. M.: Growth status of children exposed to fallout radiation on Marshall Islands.
PEDIATRICS, 36:721, 1965.
4. Conard, R. A., Rail, J. E., and Sutow, W. W.: Development of thyroid nodules as a late sequela of radioactive fallout exposure: stud-ies in a Marshall Island population exposed to fallout in 1954. Unpublished manuscript.
Dn. YAMAZAKI: Dr. Louis Hempelmann, whose long interest in radiation of the neck and chest area and its relationship to
thy-roid carcinoma has called attention to the
cautious use of x-rays to this area and
pointed to the sensitivity of the thyroid to ionizing radiation, is our next speaker.
Dn. HEMPELMANN: I shall discuss only those aspects of Dr. Miller’s excellent
pre-sentation having to do with induction of
neoplasms by exposure to ionizing
radia-tion.
First, I wish to comment on the study of
Saxon Graham and his colleagues’ which
shows that mothers of leukemic children
had a higher incidence of preconceptual
cx-posure to diagnostic x-ray procedures than
did randomly selected control women. This
association was only of borderline
sig-nificance in fathers. Such associations do
not establish a cause and effect relation-ship, but they can be useful in providing clues as to possible etiologic relationships. In particular, this association is interesting because of the small quantity of radiation involved and the implied genetic transfer of a neoplastic trait or susceptibility.
I have discussed the findings with experts in related fields. I have talked with Dr.
Phil-ip Burch of Leeds, England, who has
pro-posed a theory for the development of
childhood leukemia based upon the
inheri-tance of one prezygotic mutation followed by the occurrence of two additional specific
somatic mutations in stem cells of
blood-forming tissues.’ Dr. Burch believes that
the radiation exposure of the mothers in the
Graham study had nothing to do with the
development of leukemia in their children.’
He postulates that the mothers carrying
leukemogenic genes were “less fit” and,
therefore, had more illnesses which
re-quired radiographic procedures. This may
well be the correct interpretation but,
among geneticists, there is a strong feeling
that a leukemogenic gene would express
itself in ways other than the vague quality of being “less fit.”
I also spoke to Dr. E. B. Lewis of the
California Institute of Technology whose
studies of the quantitative risks of leukemia
as a result of radiation exposure are well
known. Dr. Lewis devised a theory to
ex-plain Dr. Graham’s results. He postulates that, for leukemia to develop, a stem cell of
blood-forming tissue must become
homozy-gous for a leukemia-producing mutant.4 If a
single leukemia-producing mutation
oc-curred in the germ line of the irradiated mother, only the second mutation occurring in the somatic cell of the offspring would
be needed for leukemia to develop.
Al-though Dr. Lewis model involves a
the low-dose region would have a strong linear component.
I am not advocating the conclusion that
radiation exposure was the cause of
leukemia in these children, but I want to
point out that the question here, as in the case of prenatal exposure, is not settled.
Therefore, we must keep an open mind.
Second, I wish to expand the subject of
radiation-induced thyroid neoplasms.
Cer-tam studies suggest that the most readily radiation-induced neoplastic process is
thy-roidal neoplasia. We found an unusually
high incidence of thyroid neoplasms as well
as of other tumors in a repeat survey of
neoplastic disease in almost 3,000 persons treated with x-rays in infancy for thymic
enlargement.’ In contrast to the tumors of
extra-thyroid origin which occur only after exposure to higher doses of x-ray
(
namely,over 200 to 300 roentgens-air dose
)
, thethyroid tumors seem to show a rather
pecu-liar dose response. Although we cannot
draw an accurate dose response curve at
this time, it seems likely that the incidence increases rapidly in the region of 50 to 200
rads absorbed thyroid dose, following
which it increases gradually. The latent
pe-riod between radiation exposure and tumor
development appears to be independent of
the dose to the thyroid gland in the dose
range studied (100 rads absorbed thyroid
dose to more than 600 rads). In persons
with thyroid doses exceeding 100 rads, the
incidence of thyroid carcinomas and
adeno-mas combined, as detected by mail survey,
was of the order of 10%. Actually, we have
reason to believe that the true incidence is considerably higher than this value. A
sys-tematic study was made of 107 persons who
received an estimated thyroid dose of 200
rads or more and who reported no thryoid
abnormalities by mail questionnaire. In this
group 20 nodular thyroid glands were
dis-covered. It seems likely, therefore, that the true incidence of thyroid neoplasms in
per-sons receiving thyroid doses in excess of
100 rads may be at least twice that
men-tioned above and, perhaps, even higher. The high incidence of thyroid neoplasms
after irradiation in childhood has also been observed in the Marshallese exposed to fall-out from a nuclear test in 1951, as reported by Dr. Sutov. \Vhy the thyroid neoplasm in-cidence in one series of irradiated children and in the Marshallese children should dif-fer so radically from that in the Japanese
atom-bomb survivors is not clear at this
time.
The clinical characteristics of tile
radia-tion-induced thyroid neoplasms observed in
our series of persons irradiated as infants are interesting.5 The peak incidence of
thy-roid carcinoma appears to occur in the 15
to 19 years of age category, where as that
for thyroid adenoma occurs later in life.
Carcinoma in the very young seems to
occur predominately in the male; five of six
cases developing before age 15 were boys.
Histologic examination of the 19 cases of
thyroid carcinoma revealed well differen-tiated adenocarcinoma. All had responded
to treatment. Even the nine cases with
me-tasteses to lymph nodes and one with
pul-monary metastasis in 1952 were living and
well in 1963. TIlls suggests that tile thyroid neoplastic process in these cases was in the
hormone-dependent stage rather than the
autonomous stage.
Finally, I wish to mention the quantita-tive risks of inducing various types of neo-plastic disease as a consequence of
radia-lion exposure. The 1964 Report of the
United Nations Scientific Committee on the
Effects of Atomic Radiation reviews all
available epidemiologic data on cancer
in-cidence in irradiated populations as a
func-tion of the radiation dosage absorbed by
the affected organ. In leukemia, thyroid
cancer, and bone sarcoma, the risks of
de-veloping malignancy turns out to be of the
same order of magnitude, namely, 1 case
per million people per rad absorbed per
year. Although the dose calculations can be criticized, particularly those concerned with bone doses, the application of correction factors modifies the risk value surprisingly
little. The similarity of the risk value in
these widely different types of neoplasms
differences in exposure conditions and in
the age, race, and other characteristics of
the exposed populations. Is this merely
coincidental? Is it due to the fact that the total incidence figures tend to obscure the incidence as a function of dose for individ-ual dose response curves? Or, is it because
there is a small sensitive subpopulation in
which all events except the final one
needed for malignant transformation have
occurred? If there is such a sensitive
sub-population, could it be that interaction of
cell lines in any tissue with the same quan-tity of radiation will produce the final event
necessary to complete the neoplastic
pro-cess?
Dr. Leonard Hamilton has made the
in-teresting suggestion that each unit of
radia-tion could have the same carcinogenic
ac-tion on all tissues.5 In those tissues which
rarely become malignant spontaneously,
the excess cases due to radiation exposure would be clearly evident, whereas in tissues
with a high spontaneous incidence the
slight excess would not be apparent.
Obvi-ousiy tilese questions cannot be answered
at the present time. However, they do pose
interesting problems, which may be
funda-mental to the evaluation of radiation
haz-ards.
In conclusion, I should like to place the
risk of inducing malignancy by radiation
exposure into proper perspective by
em-phasizrng the figure of 1/10/rad/year. The risks of persons exposed to small doses of radiation are extremely small compared
to everyday hazards; they become
impor-tant only when large populations are
in-volved.
REFERENCES
1. Graham, S., Levin, M., Lilienfeld, A., Schuman, L., Gibson, R., David, J., and Hempelmann, L. H.: Preconception, intrauterine and post-natal irradiation as related to leukemia. Nat. Cane. Inst. Monogr. 19, 347-371, 1966.
2. Burch, P. R. J.: Leukemogenesis in man. Ann.
N.Y. Acad. Sci., 114:213, 1964.
3. Burch, P. B. J.: Personal communication. 4. Lewis, E. B.: Personal communication.
5. Pifer, J. W., Hempelmann, L. H., Burke, C.,
Toyooka, E., llazeii, R., and Ames, W. H.: Neoplasms after irradiation with X-rays for thymic enlargement. I. Repeat Survey of the
Upstate New York Series in 1963.
Sub-mitted to J. Nat. Cancer Inst.
6. Report of the Unit?d Nations Scientific Corn-mittee on the effects of atomic radiation.
(Suppl. 14), (A/5814), New York: United
Nations, 1964.
7. Casarett, C. \V. : Experimental radiation car-cinogenesis. In Progress in Experimental Tu-mor Research, Vol. 7. Basel/New York: Kar-ger, pp. 49-82, 1965.
8. Hamilton, L. : Personal communication.
Dn. BRUES: I would like to ask Dr. Sutow
whether the lowered values for serum PBI
occurred at 10 years or so after the exposure or wilether that was the first time the de-termination was done.
DR. Surow: Because of this statural
re-tardation a number of PBI examinations
were done and tiley had all remained
with-in normal limits until March 1965. At that
time two of the boys showed PBI values
well within the hypothyroid range, a sharp
drop. I am not sure whether the PBI levels
reflected thyroid hormone activity or not.
\Ve have not obtained adequate growth
hormone studies. The growth hormone level
determination needs to be done on these
children to determine whetiler it is
con-cerned with statural retardation.
Dn. YAMAZAKI: In commenting on the
growth hormone, we have been impressed
with the growth retardation of rats
irradi-ated over the whole body or the head.
At-tempts to change their growth patterns
with growth hormones have been
unsuc-cessful. Thyroxine administered to these ani-mals has not changed their growth pattern.
Their nutritional intake was studied and it
too is not a factor.
Dn. KIMELDORF: We have been studying
the persistent retardation in bone growth in male rats following x-ray or fast neutron
exposure.’” Tile degree of retardation
ob-served is proportional to dose and inversely
proportional to the age of exposure. It is
possible to derive a single equation that
SUPPLEMENT \Ve have used regional exposure by x-rays
in an attempt to analyze local and
sys-temic factors involved in this ‘
Only about 50% of the total inhibition in
growth of the femur or tibia was dependent
on having tile measured bone in the
expo-sure field. Regional exposure of the head,
cilest, or abdomen would produce inhibi-tion in long bone growtll, but the amount was never equal to the total systemic effect. In the search for tile humoral mecilaflism
involved in systemic effects, we have made
chronic vascular parabiont preparations of
male litter-mate rats. We have irradiated
OI1C member of the pair and studied the
bone growth in both the irradiated and
shielded partners. We find no inhibition of
bone growtil in tile shielded animal and less
retardation in the irradiated animal. This
suggests that the inhibition of growth is not
a toxic immoral factor, since growth was
not inhibited in the shielded animal. Since
the exposed partner shows less response to
x-rays, it is suggested that an alteration in hormonal control of growth, supplemented
by the shielded partner, is responsible for the systemic effects on bone growth
inhibi-tion found in several species. Details of
these findings have been published recent-ly.6
DR. BRILL: Can any participant bring us up to date on thyroid disease in the popula-tions of Utah which are relevant to the dis-cussion?
Dn. CIADwIcK: The population studied is in the offsite area of the Nevada test site. Many of you know that the most recent phase of this endeavor has been a check of school children in the St. George area, one of the areas believed to have received some of the larger dosage from radioiodine. There is a great deal of difference of opinion as to what this dosage might have been. In order to have some basis for judging the result of
the examination of the thyroid gland,
an-other community was chosen in the
moun-tain area that had many similarities with
the St. George area, namely, Safford, Arizo-na. In general it is quite similar. We exam-ined the school children in the two
commu-nities-2,200 in tile St. George area and
1,400 in Arizona. For the screening
exam-inations physicians who were generally not
specialists in thyroid disease were trained to examine the neck to detect six specific thyroid abnormalities. Six physicians were divided into teams of three aild examined
children in both of the communities. Tile
teams of three switched communities in tlle
middle of the study. In tile two
Commum-ties there were 70 children in Utah and 25
in Arizona who required further evaluation
or had some finding suggesting a nodule.
Subsequently, tilree thyroid experts looked at the group of 70 and the group of 25
chil-dren, they found 13 in Utah who needed
clinical follow-up in a medical center to de-termine the basis for the thyroid nodularity.
In the Arizona group they found none who
needed the medical center follow-up.
The medical center follow-up Oil tile 13
children from the Utah area showed no
thy-roid cancers. The predominant finding was
thyroiditis, a lyrnphocytic infiltration of the thyroid gland. The experts, themselves, are
arguing about the significance of some of
the laboratory and clinical findings,
in-eluding biopsy studies that were done on
some of the children. With three patholo-gists in thyroid disease diverse answers may
be expected. We do know that the
abnor-malities are not cancers or adenoma, such
as were found in tile Rongelap cases.
Several things should be mentioned
about this study. First of all, the 2,200
chil-dren are not prime subjects, that is, they
are not all life-time residents of St. George.
Some are children living in St. George in
the heavy fallout period of tile early 1950’s
and some are children who have moved in
since that time. Some living there at the
time have subsequently moved elsewhere.
The estimates of exposures vary widely.
This simply reflects the fact that there was
no adequate monitoring at that time. Good
information is lacking on the dosage
re-ceived by the group in tile early 1950’s.
Most of the dose estimates are lower than
the much more precise estimates of the
268
DR. POWELL: Are we correct in assuming
that tile 13 were all in Utah in the early
1950’s.
DR. TIIosrPsoN: At least one of the 13
lived there only 1 month. I happen to know
where they lived the rest of the time and it
was in an area that could have had
expo-sure tile same as St. George. That is why
we don’t yet have the final report. The prin-cipal tiling is we do not have thyroid can-cer, but the fact of thyroiditis suggests that we have a great deal more studying to do.
DR. BUSTAD: I have a question for Dr. Sutow. This study is very interesting to me
and I have discussed it with Dr. Conani on
several occasions. I have read the reprint of the article soon to be released on this sub-ject whicil you co-authored along with Drs.
Collard and Rail.
There are two things that concern me
about this study. The first is the dose to the
children. I do not believe that even 1,500
rad to tile thyroid from radioiodine, plus
175 rad total body dose, are sufficient to
cause tile hypothyroidism manifested by
the boys. Either the dose estimations are
much too low or there are extraneous
fac-tors such as diet or organic disease, or a
combination of these factors. The second
issue relates to the diet of the children. I
am not convinced that the diet for the
chil-dren or even of all the people is adequate in stable iodine because some of the iodine
urinary excretion values reported are in the
goitrogenic range. Just because one lives by
the sea on a small island is no assurance that sufficient iodine is obtained. As evi-dence I submit the incidence of coastal goi-ter in Japan. Does Dr. Sutow have any
comments on the differences one sees in the comparative number of adenomas and car-cinomas in this and other situations? In the Marshallese children only adenomas have been observed while in the x-irradiated children described by Hempeimann and
associates and Saenger and his associates,
both adenomas and carcinomas were seen.
Do you believe radioiodine is relatively more efficient in producing adenomas and
x-ray carcinomas?
I would like to ask Dr. Chadwick about
thyroiditis. Is there any evidence you or
anyone else has over this long period of
time which suggests that thyroiditis is
radi-ation induced?
Dr. Miller, of the thyroid cancers that
you saw, how many of them were in utero
or very early in life? How many were
follic-uiar carcinoma and how many papillary? I
think there is a difference with some other groups.
DR. Si.rrow: I do not know the answer to
the question as to why we had adenomas
and why carcinomas are not found. This
goes into the realm of carcinogenesis and I
am not all prepared to discuss why the
children did not show carcinomas. One adult did.
In reference to the growth curve, the
question was whether the two markedly
re-tarded children skewed the curve so that all
of the children seemed to be retarded.
There were several other children in this
category. They contributed also as they too
were retarded, although not as markedly as
these two children.
In reference to hypothyroidism, while we
did obtain normal PBI values, we are now
wondering if this did, in truth, reflect the
degree of thyroid function. It could be we
were measuring something other than func-tioning thyroid hormone.
In reference to dose, I neglected to
men-tion the rather significant 175 rad whole body exposure. This was measured at a
level of about 3 feet above the ground and many of these children were certainly under that 3 foot level.
Dn. MILLEII: I don’t know the answer to
the question relative to frequency of
adeno-mas and carcinomas of the thyroid, but I
quoted an article published by Socolow and associates in the New England Journal of Medicine.0 In the cases reported, between
1958 and 1961,the youngest patient was 6
years old and five patients were between 6
and 16 years at the time of exposure. Some
of them had carcinomas and some had
ade-nomas, but I do not recall how many of
each. I don’t know of any case of carcinoma
SUPPLEMENT
or adenorna occurring in a child who was in
utero at the time of exposure. I asked Dr.
Sutow and he knows of none.
DR. SA.ENGER: There is one other
possibili-ty. If one looks at Hempelmann’s data and
also ours, the treated children received rel-atively iligh dose rates of gamma radiation
and perhaps more uniform distribution of
dose than did children who received
radio-iodine. These factors might explain the
differences in rates of neoplasia.
DR. BRILL: In response to Dr. Bustad’s
remarks, it should be pointed out that the
group at San Francisco has followed nine
children who had been treated for thyrotox-icosis with radioiodine and has reported the
appearance of adenomas in each of these
children. Upon detailed review, no thyroid carcinoma was found in any of tile children biopsied.
Dn. YAMAZAKI: We will close tile
discus-sion with some further obervations by Dr.
Hempelmann.
DR. HEMPELMANN: I wish to tell you
something about the latest observations in
our population of children treated with
x-rays in infancy for enlargement of the
thy-mus gland. The method of exposure of
these children is completely different from the type of exposure in fallout, but I think we do characterize some of the latent
radia-tion-induced neoplasms that might occur
after fallout. We have been following a
population of almost 3,000 persons for the
past 10 years. Their mean age in 1963 was
17 years of age. Periodically, questionnaires
were sent out among this population and
there has occurred an extremely high
inci-dence of thyroid cancer, thyroid adenoma
leukemias, osteochondroma, and other rare
tumors, such as mixed tumors of the salivary
gland and neurilemmomas. It is now quite
certain that the peak incidence for leuke-mia has passed and that the peak period for
thyroid cancer and osteochondroma has
passed. We think that the peak for the
thy-roid adenoma at age 20 has not passed,
al-though one undoubtedly misses many
things of interest by mail questionnaires.
However, when dealing with such a large
population it is feasible. One piece of
infor-mation the mail technique permits is
detec-tion of certain high-risk groups which are
apt to have neoplasm. One such risk group
of 260 children now has a total of 36
neo-plasms, of which 20 are neoplasms of the
thyroid gland.
(
Dose data is quite good.) From the information we are accumulatingon the incidence of a number of tumors, it
is hoped there can be derived some
mea-sure of the risks involved in this type of
radiation exposure and some better
mea-sure of the response. If one considers only tumors of all types which are extra thyroid and compare their incidence against the air dose, a measure relating to dose response is
obtained. The incidence after the low 200
air dose is extremely low, while that after
400 or 500 exposure is much higher,
ap-proaching an incidence of about 10%. We
have been able to calculate thyroid gland
doses in most of these children and we have also tried to assess the incidence of thyroid neoplasms as a function of the dose. I will
not attempt to draw a dose response curve
as we are not that confident of the doses. Certainly, all the incidence figures given
you are minimal figures detected by the
mail survey technique, which we know is
low by a factor of 2 and possibly a factor of 3. There is apparently a very rapid increase
in incidence following exposure in the
range of 50 to 300 rads, levelling off over
300 rads in the range of about 10% in the
people exposed. We hope to break down
this semi-qualitative dose response into the response for thyroid cancers and adenomas.
In the group of 2,300 people who have
re-ceived less than 400 rads to the thyroid,
there have been four cases of carcinoma
and 11 cases of adenomas. Whereas, in
ap-proximately 300 people who received more
than 400 rads to the thyroid, there have
been 10 carcinomas and 8 adenomas. So,
there is a suggestion that the lower doses
are more effective in producing adenomas
than carcinomas and the reverse is true of
the higher dose.
Our data show no correlation between
dose and latent period after exposure. It
looks to me like the peak incidence of
the thyroid-prone, high-risk group is mostly in their twenties at that time. The peak
in-cidence for thyroid adenomas occurs later,
but we don’t know when. Of the 19 cases of
thyroid cancer, of which 8 or 9 have
metas-tases, all are living and well and have
re-sponded favorably to treatment. I don’t
know why our findings differ from those of
Dr. Miller, nor do I know why they
resem-ble more closely the data of the
Marshall-ese. The exposure conditions in each
in-stance were so different.
REFERENCES
1. Phillips, R. D., and Kimeldorf, D. J.: The long
term effects of neutron exposure on bone
growth in the rat. Radiat. Res., 23:491, 1964. 2. Phillips, R. D., and Kirneldorf, D. J.: Acute and
long term effects of X-irradiation on skeletal growth in the rat. Amer. J. Physiol., 207:1447, 1964.
3. Phillips, R. D., and Kimeldorf, D. J.: The life span skeletal growth deficit in rats exposed to neutrons or X-rays as young adults. Radiat. Res., 22:223, 1964.
4. Phillips, B. D., and Kinieldorf, D. j.: Age and dose dependence of bone growth retardation induced by X-irradiation. Radiat. Res., 27: 384, 1966.
5. Phillips, R. D., and Kimeldorf, D. j.: Local and systemic effects of ionizing radiation on bone growth. Amer. J. Phvsiol., 210:1096, 1966. 6. Carroll, H. W., Phillips, R. D., and Kirneldorf,
